中文摘要：

目的：探讨早期凋亡T淋巴细胞的抑制性免疫调节性能。方法：采用定时紫外线照射诱导T淋巴细胞早期凋亡，深低温反复冻融获得坏死T淋巴细胞。体外诱导、纯化并培养骨髓源性不成熟树突状细胞（imDCs），imDCs分别和早期凋亡或坏死T淋巴细胞共培养。用流式细胞仪、双夹心ELISA、[^3H]掺入混合淋巴细胞反应等方法分析imDCs吞噬早期凋亡或坏死T淋巴细胞后，在不同处理条件下，MHC-Ⅱ、CD40、CD80、CD86的表达水平、分泌IL-12 p70以及刺激T淋巴细胞增殖能力的差异。结果：imDCs和坏死细胞碎片共培养后明显趋于成熟，其MHCⅡ和CD40、CD80、CD86的表达水平显著上调；分泌较高水平的IL-12 p70；和同种异体处女T淋巴细胞混合培养后显著刺激处女T淋巴细胞增殖。imDCs和早期凋亡的T淋巴细胞共培养后，其MHC-Ⅱ、CD40、CD80和CD86的表达维持较低水平；仅分泌较低水平IL-12 p70；和同种异体处女T淋巴细胞混合培养后不能刺激淋巴细胞增殖。此外，早期凋亡的T淋巴细胞孵育上清显著抑制了吞噬坏死细胞碎片后的imDCs表达共刺激分子CD40、CD80、CD86。当TGFβ1中和抗体和早期凋亡T淋巴细胞同加入imDCs，在表达MHC-Ⅱ、CD40、CD80、CD86，分泌IL-12 p70，刺激处女T淋巴细胞增殖等方面和吞噬坏死T淋巴细的DCs相比无显著差异。结论：早期凋亡T淋巴细胞通过释放免疫抑制性细胞因子TGFβ1，诱导imDCs呈现出耐受性DCs（TolDCs）的免疫表型及生物学特征，从而发挥抑制性免疫调节作用。

英文摘要：

AIM： To study the immunosuppressive effects of early apoptotic T lymphocytes. METHODS ： Early apoptotic spleen T cells were induced by ultraviolet irradiation for 5 min. After irradiation, spleen T cells were incubated at 37 ℃ with 5% CO2 for 2 h and thus early apoptotic T lymphocytes were obtained. Three to four freeze thaw cycles resulted in disruption of the spleen T cells into fragments, imdendribic cells （Des） were prepared from red cells and T cells depleted bone marrow cells. The imDCs were divided into five groups： group A： necrotic spleen T cells were added to imDCs; group B： early apoptotic spleen T cells were added to imDCs; group C： supematants from early apoptotic spleen T cells alone with necrotic spleen T cells were added to imDCs; group D： TGFβ1 neutralizing antibody along with early apoptotic T lymphocytes were added to imDCs; group E： immature dendridic cells culture in RPMI - 1640 for 5 days were used as negative control. Flow cytometry was employed to analyze the expression of MHC Ⅱ, CD40, CD80 and CD86 on DCs in each group. ELISA was employed to assay the IL - 12 p70 produced by DCs in different groups. The amounts of TGFβ1 released by early apoptotic T lymphocytes were also determined by ELISA. T cells proliferation assay was employed to study DCs＇ T cells stimulatory capacity. RESULTS： The DCs expressed high level of MHC Ⅱ , CD40, CD80 and CD86 when exposed to necrotic cells while early apoptotic cells did not. The supematants from early apoptotic spleen T cells suppressed the expression of MHC Ⅱ , CD40, CD80 and CD86 on DCs exposed to necrotic spleen T cells. When TGFβ1 neutralizing antibody along with early apoptotic spleen T were added to imDCs, the expression of MHC Ⅱ , CD40, CD80 and CD86 was increased significantly. The necrotic spleen T cells increased IL - 12 p70 production by DCs, while apoptotic spleen T cells at early stage did not （P 〈0.01, group B vs group A or B; P 〉0.05, group B vs group E）. Only the DCs that exposed to necrotic sp